ArticleFunctional & integrative genomics2025
β-Lapachone sensitizes glioblastoma to Temozolomide by inhibiting NF-κB signaling.
Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- TRIM47 promotes cell viability, cell cycle progression, metabolic reprogramming, and inhibits apoptosis of glioma via the NF-κB signaling pathway.Translational cancer research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Temozolomide (TMZ) constitutes the first-line chemotherapeutic regimen for glioblastoma (GBM), yet its clinical efficacy remains suboptimal. β-lapachone, a naturally occurring NQO1 inhibitor, has demonstrated potent antitumor activity across multiple malignancies. Based on the critical involvement of nuclear factor-κB (NF-κB) in GBM pathogenesis, this study investigated whether β-lapachone can enhance the antitumor effect of TMZ by targeting the NF-κB pathway using both in vitro and in vivo models. We found that β-lapachone acts synergistically with TMZ to inhibit GBM cell proliferation, epithelial-mesenchymal transition (EMT), and angiogenesis by suppressing NF-κB activation through blockade of p65 nuclear translocation. These results provide a solid preclinical foundation for combining β-lapachone with TMZ as a promising strategy to counteract TMZ resistance in GBM.
Indexed as
Identifiers
41331117What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.